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Patho > cardiac > Flashcards

cardiac Flashcards

1
Q

systolic BP

A

highest pressure achieved by the contraction of the L ventricle

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2
Q

diastolic BP

A

BP maintained in aorta between ejections

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3
Q

pulse pressure

A

difference between SBP and DBP

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4
Q

baroreceptors

A

send signals to brain when there are changes in BP

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5
Q

If there is a change in BP, what happens to the cardiovascular center?

A

HR increases and it vasoconstricts to increase blood flow to the heart

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6
Q

Neural and Humoral mechanisms are responsible for what type of regulation of BP? what about Renal mechanisms?

A

Short term, neural: SNS and PNS Humoral: RAA, ADH

renal: long term

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7
Q

stage 1 HTN SBP

A

140-159

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8
Q

stage 2 HTN SBP

A

> 160

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9
Q

what is the role of the sympathetic nervous system?

A

increases contractility and heart rate, induces anteriolar vasoconstriction, contributes to structural remodeling of blood vessels, renal and NA retention

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10
Q

what is the Renin-angiotensin-aldostrone system?

A

liver produces angiotensinogen which acts on kidneys which produce rennin which makes Agiotensin 1 which goes to lungs which produce ace which makes angiotensin 2 which act on adrenal glands which make aldosterone which increases NA absorption which increases BP, this also causes vasoconstriction in arterioles

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11
Q

Primary HTN

A

HTN d/t elevation in BP that is not the result of another disease process

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12
Q

Secondary HTN

A

HTN resulting from another disorder ex. kidney disease, pregnancy

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13
Q

malignant HTN

A

accelerated form of HTN DBP >120, medical emergency!

you can get cerebral edema and otic nerve swelling, H/A

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14
Q

Isolated Systolic HTN (ISH)

A

hypertension in elderly d/t stiffened arteries

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15
Q

Oslers maneuver

A

compress radial artery and if artery is palpable then its not true HTN, its pseudohypertension because arteries are stiff

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16
Q

Target Organ Disease (TOD)

A

increased workload of L ventricle which leads to heart failure, atherosclerosis develops, decreased GFR of kidneys leads to nocturia, proteninuria

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17
Q

what causes Orthostatic Hypotension

A

decrease in venous return, decreased cardiac output

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18
Q

conditions that cause orthostatic hypotention

A

dehydration, bed rest, spinal cord injury, vomiting, diarrhea, medications, autonomic nervous system disorders, aging

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19
Q

Atherosclerosis

A

hardening of arteries, lesions in arteries

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20
Q

fatty streaks, what is it made up of

A

common in all ages, contains foam cells of smooth muscle, thin, yellow that progressively enlarge

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21
Q

Fibrous Plaques, what is it made up of and what does it do

A

connective tissue, progressively thickens and occludes lumen

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22
Q

Complicated lesion, what is it made up of and what does it do

A

fibrous plaque thats soft that can rupture, contains ulcers that can crack and bleed and the forms a clot!

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23
Q

common sites for atherosclerotic lesion

A

abdominal aorta and iliac arteries, carotid arteries, thoracic aorta, femoral, popliteal arteries, coronary arteries

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24
Q

Artherosclerotic lesions: Fixed or stable plaque

A

obstructs blood flow and is implicated in stable angina

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25
Q

Artherosclerotic lesions: unstable or vulnerable plaque

A

can rupture, cause thrombus formation and is implicated in unstable angina and MI

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26
Q

what determines the vulnerability of plaque in atherosclerosis to rupture?

A

size, thickness, inflammation, lack of smooth muscle with impaired healing, thin fibrous cap

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27
Q

CAD risk factors

A

low birth weight, obesity, HTN, hyperlipidemia, smoking, family Hx, men >45, women >55

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28
Q

Hyperlipidema risk factors

A

cholesterol >200, dietary, genetic,alcoholism, hypothyroidism, corticosteriods, estrogens

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29
Q

Homocysteine

A

promotes progression of atherosclerosis by causing endothelial damage and increases LDL and smooth muscle growth

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30
Q

who should be screened for high levels of Homocysteine?

A

unusual family hx, poor nutritional status, unexplained atherosclerosis deposits

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31
Q

major complications of atherosclerosis

A

Ischemic heart disease, Stroke, PVD

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32
Q

Coronary heart disease: Chronic Ischemic heart disease

A

chronic stable angina, silent heart ischemia and varient vasospastic angina

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33
Q

Coronary heart disease: Acute coronary syndrome

A

NSTEMI, STEMI

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34
Q

Coronary Artery Disease

A

narrowing of the coronary arteries d/t atherosclerosis

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35
Q

Coronary Artery disease affect on the heart and what does it lead to

A

it blocks the oxygen supply to heart tissue which leads to HTN, angina, hysrhythmias, MIs, CHF

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36
Q

Collateral circulation

A

growing new vessels to supply organs

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37
Q

what do you see on an EKG with CAD with ischemia? during MI?

A

ischemia: ST or T wave depression
MI: ST elevation, T wave depression

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38
Q

which hour are you hypercoagulable which leads to the most MIs?

A

6am

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39
Q

1 Sudden cardiac death cause

A

because of lethal dysrhythmias

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40
Q

unstable angina and causes

A

recent onset, change in pattern

causes: atherosclerotic plaque disruption, platelet aggregation, secondary hemostasis

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41
Q

stable angina and causes

A

constant pattern of pain and severity

causes: coronary stenosis

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42
Q

Variant (Printzmetals angina) and causes

A

rest pain and V-arrhythmias cause by carotid artery spasm,

causes: drug abusers, coronary vasospasm

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43
Q

Angina heart sounds

A

split S2 on expiration, S4, S3, systolic murmur

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44
Q

how many days until granulation tissue forms after an AMI?

A

8-10 days

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45
Q

how long after an AMI does infarct turn gray with yellow streaks?

A

48 hrs

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46
Q

how long after an AMI does necrotic area develop into a scar?

A

2-3 months

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47
Q

the size of an AMI depends on what?

A

extent, severity, duration, amount of collateral circulation, metabolic needs of the heart at the time of the event

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48
Q

anterior or septal MI occurs when which artery is obstructed?

A

left anterior artery (LAD)

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49
Q

lateral wall MI occurs when which artery is obstructed?

A

circumflex artery

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50
Q

Inferior/posterior wall MI occurs when which artery is obstructed?

A

right coronary artery (RCA)

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51
Q

Subendocardial infarcts, what does it involve and when does it occur

A

involve 1/2 of ventricular wall, occur when arteries are narrow but patent

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52
Q

Transmural infarcts, what does it involve and when does it occur

A

involve full thickness of ventricular wall, occur when there is obstruction of a single artery

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53
Q

does myocardial regenerate?

A

NO, damaged tissue is replaced by scar tissue

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54
Q

1 mm ST segment elevation in 2 contiguous leads is indicative of what?

A

AMI

55
Q

Creatinine Phosphokinase (CPK), where is it found?
CK-MM
CK-MB
CK-BB

A

enzyme found in heart (MB), brain(MM) and skeletal muscle(BB)

56
Q

LDH1 and LDH 2

A

enzymes used to detect heart damage

57
Q

Diagnostic gold standard to detect MI

A

Troponin 1

58
Q

Thallium Scans

A

assess ischemia or necrotic muscle tissue

59
Q

MUGA scans

A

to evaluate L ventricular function

60
Q

what kind of rub do you hear with ischemic pericarditis

A

pericardial friction rub

61
Q

cardiac output

A

amount of blood the heart pumps each minute (L/min)

62
Q

what does the sympathetic nervous do to the heart rate

A

increases it

63
Q

what does the parasympathetic nervous do to the heart rate

A

decreases it

64
Q

stroke volume

A

amount of blood the heart pumps with each beat

65
Q

cardiac reserve

A

maximum percentage of increase in cardiac output achieved above normal resting level

66
Q

aortic impedence

A

loss of elasticity of aortic wall (this increases with aging)

67
Q

what happens to the left ventricle with aortic impedance?

A

the left ventricle must generate higher pressure to get blood through

68
Q

starlings law

A

the degree to which the heart muscle can stretch

69
Q

preload

A

volume of blood the heart pumps out

70
Q

after load

A

the pressure it must generate to pump the blood out of the heart

71
Q

myocardial contractility and its most important factor in what?

A

force of contraction

important factor: ventricular performance!!

72
Q

what happens to the heart according to starlings law with heart failure?

A

there is an increase in muscle stretch but no increase in force of contraction, (a floppy muscle)

73
Q

heart compliance

A

the ease with which the heart relaxes as it fills with blood

74
Q

what will an echo look like with a patient who has systolic heart failure?

A

it will have a floppy muscle

75
Q

How do we prevent the heart muscle from becoming floppy with systolic heart failure?

A

lower the BP

76
Q

aortic stenosis and HTN effect on after load

A

it increases it

77
Q

what does an increased after load do to the heart?

A

It increases the workload and oxygen consumption

78
Q

if myocardial contractility is increased, what happens to amount of blood that is ejected?

A

its increased

79
Q

if myocardial contractility is increased, what happens to the systolic ejection fraction?

A

it increases

80
Q

if myocardial contractility is increased, what happens to the end systolic volume?

A

it decreases

81
Q

if myocardial contractility is decreased, what happens to amount of blood that is ejected?

A

it decreases

82
Q

if myocardial contractility is decreased, what happens to the systolic ejection fraction?

A

it decreases

83
Q

if myocardial contractility is decreased, what happens to the end systolic volume?

A

it increases

84
Q

what is dependent on the concentration of catecholamines in the heart muscle

A

myocardial contractility

85
Q

what is the myocardial contractility influenced by?

A

preload, after load and SNS stimulation

86
Q

negative inotropic effects on the heart (3) and what do they do to it?

A

hypoxemia of the heart, hypercapnia of the heart, academia (acidosis) of the heart——IT DEPRESSES THE HEART so it can’t work!

87
Q

inotropic

A

agent that affects the heart speed of force of contraction

88
Q

which stretches more easily and which works under pressure? veins or arteries

A

veins: stretch
Arteries: work under pressure

89
Q

stroke volume

A

amount of blood ejected with each ventricular contraction

90
Q

End-diastolic volume

A

total volume in L ventricle at end of filling just prior to contraction

91
Q

End-systolic volume

A

total volume in L ventricle at the end of the contraction

92
Q

EF

A

percent volume of blood ejected with each ventricle contraction

93
Q

1 cause of heart failure

A

atherosclerosis

94
Q

Ischemic heart disease (CAD), AMI, cardiomyopathy, myocarditis, constrictive pericarditis, congenital heart defects are all causes of what kind of heart failure

A

Intrinsic

95
Q

COPD, pulmonary embolism, hyperthyroidism, HTN, AV fistulas, drug toxicities are all causes of what kind of heart failure?

A

secondary

96
Q

With heart failure there is a decrease in cardiac output, what compensatory responses do you get with this?

A

SNS increases HR, kidneys release HR to increase BP, anaerobic metabolism and increased oxygen extraction by peripheral cells

97
Q

what happens to heart muscle with systolic heart failure

A

L ventricular muscle is stretched out and floppy

98
Q

what happens to heart muscle with diastolic heart failure?

A

muscle hypertrophy (heart muscle is bigger causing a decrease in L ventricular chamber size)

99
Q

high out put heart failure is which kind of heart failure?

A

diastolic heart failure

100
Q

low out put heart failure is which kind heart failure?

A

systolic heart failure

101
Q

whats the treatment for low output heart failure or systolic heart failure?

A

diuretics

102
Q

Left sided heart failure represents?

A

failure of the left side of the heart to move blood from the lungs to the circulatory system

103
Q

causes of left sided heart failure

A

AMI, systemic HTN, cardiomyopathy, aortic stenosis

104
Q

Because blood backs up into lungs with left sided heart failure, (backward effect) what can you get from this?

A

pulmonary edema

105
Q

because blood is not going to the circulatory system with left sided heart failure (forward effect), what compensatory mechanism kick in?

A

SV decreases and RAA and SNS kick in to try and get HR and BP up which makes the heart failure worse!

106
Q

why does SOB and cyanosis occur with pulmonary edema?

A

because lungs are not able to oxygenate the blood so the blood leaves the lungs without being oxygenated

107
Q

Right sided heart failure represents?

A

failure of the right side of the heart to move blood from the circulatory system to the lungs

108
Q

because right sided heart failure isn’t able to pump blood to lungs, what do you get from this?

A

it causes peripheral edema and congestion of abdominal organs

109
Q

1 major cause of right sided heart failure?

A

left ventricular failure d/t excessive pressures in the pulmonary capillary bed

110
Q

besides left ventricular failure as the major cause of right sided heart failure, what are other causes of right sided heart failure?

A

cor pulmonale, COPD, PE, valve disease, Right coronary artery infarct, cardiomyopathy

111
Q

what major organ is affected with R sided heart failure? and what do you get because of it?

A

the Liver which causes ascites

112
Q

s/s right sided HF

A

JVD, plural effusions, hepatomegaly, hypoalbuminemia, resp symptoms only if have lung disease, dependent edema after first 10 lbs gain

113
Q

Biventricular heart failure

A

L to R heart failure

right doesn’t cause left but left can cause right

114
Q

causes of systolic heart failure

A

AMI, CAD, valve disease

115
Q

causes of diastolic heart disease

A

HTN, COPD, pulmonary HTN, aortic stenosis, pulmonic stenosis

116
Q

class 1 heart disease

A

patients don’t have any limitations in physical activity

117
Q

class 2 heart disease

A

patients have slight limitations of physical activity

118
Q

class 3 heart disease

A

patients have marked limitation of physical activity

119
Q

class 4 heart disease

A

patients have unable to carry out physical activity without discomfort

120
Q

congestive cardiomyopathy

A

associated with hyperthyriodism, alcoholism, childbirth

121
Q

restrictive cardiomyopathy

A

heart becomes infiltrated with abnormal substances causing extensive fibrosis

122
Q

hypertrophic cardiomyopathy

A

hypertrophy of septum which causes an obstruction of outflow of blood

123
Q

myocarditis cardiomyopathy

A

infection from viruses, inflammation from chemo

124
Q

Chords tendinae

A

connect valve leaflets to muscles, help keep leaflets closed under pressure

125
Q

papillary muscle

A

extension of the heart muscle that pull valves together to prevent back flow

126
Q

valvular heart disease

A

occurs when heart valves can’t fully open or close

127
Q

grade 1 murmur

A

soft, heard only under quiet conditions

128
Q

grade 2 murmur

A

soft, heard under even noises conditions

129
Q

grade 3 murmur

A

easily heard, prominent

130
Q

grade 4 murmur

A

loud, associated with a thrill

131
Q

grade 5 murmur

A

loud, with stethoscope tilted against chest with thrill

132
Q

grade 6 murmur

A

very loud with thrill

133
Q

diastolic murmurs are only graded to?

A

grade 4

Patho (20 decks)

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